| Project/Area Number |
22791651
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Ophthalmology
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 神経再生 / 視神経 / 網膜 / 接着因子 / ラミニン / 接着斑キナーゼ / Akt1 / 緑内障 / 神経生存 / プルプリン / 細胞外マトリックス |
|---|
| Research Abstract |
In our strategies toward optic nerve regeneration of mammals using fish derived molecule, we used purpurin(a novel extracellular matrix protein) overexpression systems by adeno-associated virus vector in rat retina. In rat, supply of purpurin could protect retinal ganglion cells(RGCs) from injury-induced apoptosis through a mechanism of focal adhesion kinase(FAK)/Akt activation. Furthermore, purpurin had adhesive effect on rat RGCs from culture study with purpurin-coated dishes. We focused on the extracellular matrix-related molecules as a mechanism of purpurin adhesive and survival effects. Purpurin inhibited optic injury-induced matrix metalloprotease 9 activity and the degradation of laminin and activated FAK signaling. Purpurin could potentially offer new avenues for developing treatments for human retinal degenerative disorders such as glaucoma.
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